CHOLINESTERASE-INHIBITORS DO NOT PROLONG NEUROMUSCULAR BLOCK PRODUCEDBY MIVACURIUM

Cholinesterase inhibitors antagonize neuromuscular block produced by m ivacurium, but some may also decrease its metabolism by inhibiting pse udocholinesterase. These opposing interactions were examined in rats a naesthetized with pentobarbitone. After spontaneous recovery from an i nitial bolus dose of 0.03 mg kg(-1), mivacurium was infused to produce 80-90% block of gastrocnemius muscle twitch. After 15 min, the infusi on was discontinued and saline, edrophonium, pyridostigmine or neostig mine was administered. Fifteen minutes later, a second bolus dose of m ivacurium was given. Edrophonium, pyridostigmine and neostigmine reduc ed the subsequent maximum block, compared with the change in saline co ntrol, by 3%, 19% and 35%, respectively. Correspondingly, the time to recovery of T1 to 50% was decreased by 20%, 58% and 62%. in rats, acer ylcholinesterase-mediated antagonism of neuromuscular block predominat ed over decreased pseudocholinesterase-mediated metabolism, such that prior administration of a cholinesterase inhibitor did not prolong the neuromuscular blocking effects of mivacurium.